Differentiating H. pylori Infection from GERD
Start with an empiric 4-8 week trial of once-daily PPI therapy if you have typical heartburn or regurgitation symptoms, but if symptoms are atypical (chronic cough, hoarseness, chest pain) or persist after PPI trial, proceed directly to upper endoscopy with gastric biopsies to simultaneously evaluate for both H. pylori infection and GERD-related mucosal changes. 1, 2
Initial Clinical Assessment
The key distinction lies in recognizing that these conditions frequently coexist—44% of patients with H. pylori-related duodenal ulcers also have GERD—so you cannot assume one excludes the other. 3
Symptom Patterns That Guide Your Approach
Typical GERD symptoms (heartburn, regurgitation worsening after meals or when lying down) warrant an empiric PPI trial first, with 71-78% sensitivity and 41-54% specificity for objective GERD. 1, 2
Atypical symptoms (chronic cough, laryngitis, chest pain, asthma, dental erosions) occur more frequently with H. pylori infection and should prompt early objective testing rather than empiric PPI therapy, because 50-60% of these patients do not actually have GERD. 2, 4, 5
Nausea and chronic laryngitis are significantly more common with antrum-predominant H. pylori infection, providing a clinical clue toward bacterial etiology. 6
Exclude cardiac causes first if chest pain is present—ischemic heart disease carries substantially greater morbidity and mortality than either GERD or H. pylori. 1
Diagnostic Testing Algorithm
Step 1: Upper Endoscopy with Gastric Biopsies
Upper endoscopy is your most efficient single test because it simultaneously evaluates for erosive esophagitis (confirming GERD), Barrett's esophagus, and allows gastric biopsies from both antrum and corpus to diagnose H. pylori infection and assess gastritis distribution. 2, 6
Perform endoscopy first in patients with atypical symptoms, alarm features (dysphagia, weight loss), or after failed PPI trial of 8-12 weeks. 1, 2
A normal endoscopy does not exclude GERD—50-70% of GERD patients have non-erosive reflux disease (NERD) requiring pH monitoring for diagnosis. 2, 4
Gastric biopsies should sample both antrum and corpus because antrum-predominant H. pylori infection may cause different clinical manifestations than corpus-predominant infection. 6
Step 2: Ambulatory pH-Impedance Monitoring (If Endoscopy Is Normal)
If endoscopy shows no erosive esophagitis but symptoms persist, perform 96-hour wireless pH monitoring off PPI therapy to definitively diagnose or exclude pathologic acid exposure. 1, 2
pH monitoring is the gold standard for diagnosing non-erosive reflux disease, which accounts for approximately 60% of GERD patients. 1
Combined pH-impedance monitoring detects both acid and non-acid reflux events, providing comprehensive assessment of reflux burden and symptom-reflux correlation using Symptom Association Probability (SAP) and Symptom Index (SI). 2
Perform pH monitoring off acid suppressive therapy for initial diagnosis—normative data interpretation while on PPI is unclear and may miss acid reflux. 1, 2
Step 3: Esophageal Manometry (Before Anti-Reflux Surgery)
High-resolution esophageal manometry is mandatory before considering anti-reflux surgery to confirm adequate peristalsis and exclude achalasia or other major motility disorders that can mimic GERD. 2
- H. pylori infection, particularly antrum-predominant, may cause subtle slowing of esophageal peristalsis (reduced contraction front velocity) without affecting reflux burden, representing early functional impairment. 6
Critical Interpretation Points
H. pylori Does Not Protect Against or Cause GERD
H. pylori infection does not affect oesophageal acid exposure time, DeMeester scores, or the number of reflux episodes—the prevalence is identical (31%) in both GERD patients and healthy controls. 6, 7
H. pylori-positive patients actually have significantly less severe oesophagitis and no patients with Barrett's esophagus are H. pylori-positive, suggesting mild protective effect against severe complications. 8
The 44% coexistence rate of GERD in H. pylori duodenal ulcer patients likely represents unmasking of pre-existing GERD after lifestyle changes and antacid discontinuation, not de novo development. 3
PPI Response Does Not Confirm Either Diagnosis
Symptom improvement on PPI therapy may result from placebo effects (present in both conditions) or mechanisms other than acid suppression, and should not be regarded as confirmation of GERD. 9, 2
- If symptoms persist after one 12-week PPI trial, additional trials of different PPIs are low yield—proceed to objective testing rather than empiric switching. 9, 2
Treatment Decision Framework
Routine H. pylori eradication in GERD patients is not necessary solely based on reflux parameters, but treatment decisions should be individualized based on:
- Presence of peptic ulcers on endoscopy 6
- Premalignant gastric lesions (atrophic gastritis, intestinal metaplasia) 6
- Family history of gastric malignancy 6
- Persistent dyspepsia despite GERD treatment 6
After H. pylori eradication, atypical GERD symptoms tend to decrease, and patients with eradication more than 6 months prior show clinical behavior similar to H. pylori-negative subjects. 5
Key Pitfalls to Avoid
Do not assume atypical symptoms are GERD-related without objective evidence—up to 60% are unrelated, and H. pylori may be the actual cause. 2, 4
Do not rely on laryngoscopy findings (erythema, edema) to confirm extraesophageal reflux—these lack specificity and inter-rater reliability. 4
Do not skip gastric biopsies during endoscopy if you suspect H. pylori—clinical symptoms alone cannot reliably differentiate the two conditions. 6, 5
Do not perform upper GI barium studies to diagnose GERD—they are too brief to rule out pathologic reflux and have high false-positive rates from physiologic reflux during the exam. 9
Do not continue empiric PPI therapy beyond 12 months without objective confirmation of GERD, as 50-60% of suspected GERD patients will not have pathologic reflux. 1